Connective tissue growth factor reacts as an IL - World Journal of ...

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A B CTGF luciferase activity (lcps) D E CTGF β-actin CTGF/β-actin (%) α1-AT β-actin IL-6 (μg/L) 0 0.05 0.1 1.0 10 100 CTGF β-actin 1600 1200 800 400 0 150 100 50 0 a a 0 0.1 1.0 10 100 0 0.1 1.0 10 100 IL-2 (μg/L) WJG|www.wjgnet.com a IL-6 (μg/L) 0.01 1.0 10 0 a 0 0.1 1.0 5 10 IL-6 (μg/L) Gressner OA et al . CTGF is a negative acute phase protein CTGF/β-actin (%) C α1-antitrypsin/β-actin (%) CTGF β-actin CTGF/β-actin (%) 120 80 40 IL-6 (μg/L) 0.01 1.0 10 0 H2O CTGF rS6 RPLO 0 160 120 80 40 0 150 100 50 0 a b b 0.01 1.0 10 0 IL-6 (μg/L) 0 0.1 0.5 1.0 10 0 0.1 0.5 1.0 10 100 IL-12 (μg/L) 155 January 14, 2011|Volume 17|Issue 2| b 0 0.1 1.0 10 100 IL-6 (μg/L) Figure 1 Interleukin-6 inhibits CYR61/CTGF/NOV 2/connective tissue growth factor expression in cultured rat hepatocytes. A: Western blotting of CYR61-CTGF- NOV (CCN) 2/connective tissue growth factor (CTGF) of rat hepatocytes (PC) cultured for 24 h under serum-free conditions with or without addition of indicated concen- a a
A Gressner OA et al . CTGF is a negative acute phase protein trations of rr interleukin (rrIL)-6. β-actin served as loading control. A representative blot is shown. Blots were quantified relative to β-actin using the Lumi Imager System. Quantifications represent the mean ± SD of 3 independent cultures. a P < 0.05, b P < 0.0001 vs untreated control; B: CCN2/CTGF reporter gene activation. Rat PC were cultured in serum-free medium for 24 h and transfected with Ad-hCTGF-Luc then subjected to the indicated concentrations of rrIL-6 16 h after transfection and cultured for another 24 h before harvest. Mean values (± SD from 3 cultures) are shown. a P < 0.05 vs untreated control; C: Reverse-transcriptase polymerase chain reaction (RT-PCR) of CCN2/CTGF of rat PC. Rat PC were cultured in serum-free medium and treated with rrIL-6 at indicated concentrations for 24 h. RT-PCR was performed using primers for rat CCN2/CTGF as described in Materials and Methods. rS6 and RPLO served as internal control. A representative experiment of 3 independent cultures is shown; D: Western blotting of α1-AT of rat PC cultured for 24 h under serum-free conditions with or without addition of indicated concentrations of rrIL-6. A representative blot is shown. Blots were quantified as described in (A). a P < 0.05 vs untreated control; E: Western blottings of CCN2/CTGF of PC cultured for 24 h in serum-free medium with or without addition of indicated concentrations of IL-2 or IL-12. β-actin served as loading control. Representative blots of 3 independent experiments are shown. Blots were quantified as described in (A). CTGF β-actin IL-6 (μg/L) 0 0.01 0.1 1.0 10 CTGF β-actin TGFβ - + + + + + IL-6 (μg/L) - - 0.01 0.1 1.0 10 B 1 2 4 24 h C CTGF β-actin CCN2/CTGF, the signal transduction pathway known to mediate IL-6 specific effects to the nucleus was interrupted at different levels using specific inhibitors (Figure 4). Inhibition of MAP-kinase signaling by the specific inhibitors (PD98059, SB203580, and UO126) did not abrogate the inhibitory effects of IL-6 on hepatocellular CCN2/ CTGF synthesis (Figure 4A). Also, blocking of phosphatidylinositol phospholipase C signaling by administration WJG|www.wjgnet.com Control IL-6 (10 μg/L) TGFβ (1 μg/L) IL-6 (10 μg/L) + TGFβ (1 μg/L) CTGF/β-actin (x-fold increase) 3 2 1 b a a 0 TGFβ (1 μg/L) - + - + - + - + IL-6 (μg/L) - - 0.1 1 10 IL-6 (10 μg/L) - + - + TGFβ (1 μg/L) - - + + p-Smad2 Smad2 p-Smad1 p-Smad3 Figure 2 Interleukin-6 acts as an inhibitor of transforming growth factor β1 induced CYR61/CTGF/NOV 2/connective tissue growth factor protein expression in cultured rat hepatocytes. A: Western blottings of CYR61/CTGF/NOV (CCN) 2/connective tissue growth factor (CTGF) of rat hepatocytes (PC) cultured under serum-free conditions with or without addition of rr interleukin (rrIL)-6 at indicated concentrations 30 min prior addition of rhTGFβ1 (1 μg/L). The cell culture only with IL-6 at indicated concentrations served as internal control. Cells were harvested after another 24 h. β-actin served as loading control. Representative blots are shown. Blots were quantified relative to β-actin using the Lumi Imager System. Quantifications represent the mean ± SD of 3 independent cultures. a P < 0.05, b P < 0.0001 vs untreated control; B: Western blottings of CCN2/CTGF of rat PC cultured as stated in (A) under serum-free conditions with or without addition of rrIL-6 (10 μg/L) 30 min prior addition of rhTGFβ1 (1 μg/L) where indicated. The cells were harvested after 1, 2, 4 and 24 h. β-actin served as loading control. A representative blot of 3 independent experiments is shown; C: Western blottings of phosphorylated and total Smad2 and Smad3, the latter antibody cross-reacting with Smad1. Rat PC were cultured for 24 h under serum-free conditions with or without addition of rh transforming growth factor (TGF) β1 (1 μg/L) and indicated concentrations of rrIL-6. Representative blots are shown. Smad3 β-actin of edelfosine did not interfere with IL-6 signaling to the CCN2/CTGF promoter (Figure 4A). However, exposure of cells to rrIL-6 leads to an activation of the JAK/STAT3 pathway by inducing STAT3 phosphorylation in primary rat PC [33] . PC were pre-treated with pyrrolidine dithiocarbamate (PDTC) for 2 h and subsequently stimulated with rrIL-6. PDTC was previously proven to primarily impair STAT3 phosphorylation in 156 January 14, 2011|Volume 17|Issue 2| b
Page 1 and 2: World Journal of Gastroenterology W
Page 3 and 4: Robert JL Fraser, Daw Park Jacob Ge
Page 5 and 6: Italy Donato F Altomare, Bari Piero
Page 7 and 8: Fernando Azpiroz, Barcelona Ramon B
Page 9 and 10: S Contents EDITORIAL TOPIC HIGHLIGH
Page 11 and 12: Contents APPENDIX FLYLEAF EDITORS F
Page 13 and 14: Ouyang D et al . Pancreatic endocri
Page 19 and 20: Online Submissions: http://www.wjgn
Page 21 and 22: Diamantis G et al . Quality of life
Page 27: Gressner OA et al . CTGF is a negat
Page 32 and 33: A B IL-6 (35 μg/L) - - + + + + - s
Page 34 and 35: F mt distal mt proximal wt 9 8 7 6
Page 36 and 37: + CTGF TGF-β IL-6 + - + an acute p
Page 38 and 39: 2007; 46: 295-303 21 Karger A, Fitz
Page 40 and 41: 2011; 17(2): 164-173 Available from
Page 43 and 44: A B C -80 mV E Relative expression
Page 45: A C Park KS et al . Serotonergic si
Page 48 and 49: 19 Li T, Weng SG, Leng XS, Peng JR,
Page 50 and 51: Recurrent GB cancer has been report
Page 52 and 53: Table 2 Surgical procedures for muc
Page 54 and 55: esection of the common bile duct sh
Page 58 and 59: NaF, 1% Triton X-100, and 0.5 mmol/
Page 60 and 61: A Oxaliplatin LY294002 C Oxaliplati
Page 62 and 63: A Tumor volume (mm 3 ) C 5000 4000
Page 64 and 65: 2 Hundahl SA, Phillips JL, Menck HR
Page 68 and 69: the typical MII pattern of GOR. Thi
Page 70 and 71: emptying, that arises from the anch
Page 74 and 75: medical treatment, age at diagnosis
Page 76 and 77: Table 3 Odds ratio for the studied
Page 78 and 79: Table 6 Published associations betw
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anti-CBir1 and ASCA, and show reduc
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Faria GR et al . Acute diverticulit
Page 88 and 89:
Online Submissions: http://www.wjgn
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Changes in flow vs T0 (%) Changes i
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Hanssen SJ et al . Hemolysis and in
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Kuiper P et al . Angiogenic markers
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Kuiper P et al . Angiogenic markers
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A Comulative survival C Comulative
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Nishida U et al . ASA induced small
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Nishida U et al . ASA induced small
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Okano K et al . FDG-PET small pancr
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Okano K et al . FDG-PET small pancr
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Table 3 Prevalence of IgG anti-hepa
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1005-1022 24 Hendrickx G, Van Herck
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Choi YS et al . Alternative cleansi
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Plasma endotoxin (EU/L) Small intes
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Zhang Y et al . Effects of penehycl
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C Review: CYP1A1 Ile462Val polymorp
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Kim SO et al . Sorafenib-induced sp
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Sahebkar A. Ginger as a natural sup
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